Abstract

To investigate the possible role of apoptosis on brief distensions of human saphenous veins at different pressures. Fresh isolated grafts of human saphenous vein were assigned as control or distended (D) for fifteen seconds at 100, 200 and 300 mmHg. The degree of apoptotic caspases 3, 8, 9 and anti-apoptotic protein Bcl-2 expression were assessed by immunohistochemistry. Fresh isolated segments of distended human saphenous veins presented similar apoptotic protein expression when compared with control veins. However, the Bcl-2 expression was significantly higher in the 300 mmHg distended segments compared with the control vein. These findings show that intact segments of human saphenous veins submitted to distensions at different pressures have similar apoptotic proteins expression when compared with non-distended control veins. Therefore, brief distensions commonly performed during surgical harvesting do not trigger apoptosis, and probably are not involved on the physiopathological mechanisms that lead to graft failure.

Highlights

  • Widely used as vascular conduit in coronary and peripheral revascularization surgery, saphenous vein grafts have shorter patency than arterial ones

  • One possible explanation for this fact is that exposition of saphenous vein to high pressures induces functional and morphological alterations that can trigger physiopathological mechanism, which lead to early thrombosis and graft failure

  • The results of this study reveal that fresh isolated segments of saphenous veins submitted to distension at 100 to 300 mmHg for fifteen seconds, presented similar expression of pro-apoptotic proteins when compared with control

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Summary

Introduction

Widely used as vascular conduit in coronary and peripheral revascularization surgery, saphenous vein grafts have shorter patency than arterial ones. One possible explanation for this fact is that exposition of saphenous vein to high pressures induces functional and morphological alterations that can trigger physiopathological mechanism, which lead to early thrombosis and graft failure. Apoptosis is one described mechanism in failing saphenous vein graft physiopathogy. It is involved in intimal layer modification with muscular layer thickening through fibrous transformations [2]. Pressure distensions and apoptosis may have clinical and experimental implications in endothelial function and, by consequence, in the use of the saphenous vein as arterial graft [3]

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